Pathological morphology - degenerations, necrosis continued Flashcards
Parenchymal fatty degenerations are
change disorders of cytoplasm fat.
This degeneration can cause an increase of fat in the cell cytoplasm of these parenchymal organs, which contain small amounts of fat in normal conditions (liver, kidneys), or fat appears in the cytoplasm of cells of organs, where it is absent in normal conditions (cardiac muscles, skeleton muscles, nerve tissue etc.).
Fat of abnormal chemical composition may form in cells as a result of pathological synthesis.
Parenchymal fatty degeneration mostly occurs in
the liver, kidneys and myocardium.
Parenchymal fatty degenerations are caused by (3)
1) several contagious diseases (sepsis, tuberculosis etc.) and intoxications
2) deficiency of carbohydrates and proteins, as well as lipotropic substances (choline,
methionine, glyco-amino acids, vitamin B12 etc.
3) oxygen deficiency in tissues, caused by lung and cardiovascular conditions, blood
circulation disturbances, anemia.
With liver fatty degeneration,
small droplets of fat appear in the peripheral part of cytoplasm of hepatocytes.
The droplets relocate then to the centre and join. Finally the whole cell can fill with fat and resemble a big fat vacuoles.
With fatty degenerations the cell nucleus is damaged and symptoms of pyknosis, or lysis in more rare cases, develop. Therefore fatty
degenerations mean that fat will deposit in damaged cells.
Liver fatty degeneration is different from
physiological fat infiltration - in that case fat drops can be found in liver cells with histological methods.
Physiological fat infiltration occurs, when the liver cells are unable to process the excess fat transported to the liver by blood
and lymph and it deposits partly to cytoplasm and is consumed later by liver cells. In this case fat will deposit in unharmed cells (no changes in cell
nuclei).
In cardiac muscles, fatty degeneration is often focal. Fat deposits in
the sarcoplasm of muscle fibres. Macroscopically such focal deposits display as greyish-yellow stripes.
Cardiac muscle, viewed from the endocardium,
resembles tiger skin, with greyish yellow and brown stripes (“tiger heart”).
With renal fatty degeneration, fat will deposit in
the epithelial cells of renal tubes.
Kidneys will expand, be bigger in volume, greyish yellow, no clear-cut border between the cortex and medulla, with oily cross-section surfaces.
Mesenchymal fatty degenerations are
neutral metabolism disturbances.
Deposits of neutral fat may decrease or increase in fat depots and the stroma of several organs and lead to cachexia or obesity.
Cachexia (cachexia) is
loss of fat in fatty tissues simultaneously with
loss of free fat in organs to a bigger or smaller extent.
The causes may be starvation (alimentary fatty degeneration), also chronic debilitating contagious diseases, parasitic diseases, non-contagious diseases
(gastroenteritis, pneumonia, tumors etc).
Fat disappears from fatty tissues, which absorb serous liquid, become slimy and gelatinous, yellowish gray.
Glycoproteinosis
Carbohydrate degenerations are carbohydrate (polysaccharide, incl. glycogen, mucopolysaccharides and glycoproteins) metabolic disorders, resulting in changes of their amount and composition.
Carbohydrate metabolic disorders are best seen with
diabetes (diabetes mellitus).
The cause of diabetes is an organism’s deficiency or lack of the hormone insulin that regulates carbohydrate metabolism, glycogen depositing in tissues and organs, where it is not present in normal conditions.
Lack of insulin disturbs glycogen synthesis in muscle and fatty tissues. Glycogen deposits decrease dramatically in tissues, especially liver, where glycogen disappears totally, the liver infiltrates with fat and fatty
degeneration develops.
At the same time epithelial cells of renal tubes,
especially the loop of Henle, infiltrates with glycogen.
When the amount of glycogen builds up in cells and abnormal accumulation of glycogen appears in tissues (liver, kidneys, smooth and skeletal muscles and myocardium), the condition is called
glycogenosis or Glycogen storage disease
concrement formation
a hard lump produced by the concretion of mineral salts; found in hollow organs or ducts of the body.
petrification
also known as calcification
Calcium metabolism disturbance that causes dissolved calcium salts depositing in tissues.
The result of calcium salt deposits in tissues is concretion or calculus.
According to the underlying mechanism of calcification, two forms can be specified:
metastatic calcification and dystrophic calcification.
lime metastases
also known as Metastatic calcification occurs with general calcium metabolism disturbances and is of general character. With metastatic calcification the
salts deposit in various tissues which might be absolutely normal and healthy.
The main cause for that is hypercalcemia, which in turn can be caused by increased loss of salts from bone or disturbances in endocrine calcium salts metabolism. That is the reason why calcium metastases occur with brittle bones.
Dystrophic calcification is
pathologic accumulation of calcium salts in tissues, where metabolism has weakened or stopped. It is focal calcification; the amount of calcium salts in blood and tissue fluids has not increased.
Calcium salts accumulate in necrotic or degenerated tissues. This type of calcium salts accumulation can be a sign of self-defence of an organism.
Calcium salts may deposit around dead parasites in tissues (calcified parasite nodules), walls of blood vessels (arterial sclerosis), foci of tuberculous caseous necrosis, also dead fetuses in uterus or abdominal cavity.
lithopedion
calcified fetus, usually extrauterine
calculi, stones or concrements are deposits of calcareous material in cavities or ducts of organs.
According to the causes of formation, they are classified as
metabolic, inflammatory and obstruction concrements.
The concrements of the digestive tract are classified as real stones (calculi veri), and pseudostones (pseudoliythiases, calculi spurii) and bezoars
(bezoaria).
“Real stones”/calculi veri are
intestinal concretions or enteroliths that consist mainly of mineral salts, are layered and have a nidus (a small
foreign object – a speck of wire, a pebble, a coin etc.) with mineral salts built up in thin layers around them.
They are round and look like cobbles, smooth or rough, also their weight resembles real stones. The cross section shows they are radial (crystallised stones). Such stones form in the colon of horses mostly, but may occur with cattle as well.
Kidney and urinary calculus, bilestones, salivary stones are real stones as well.
nephrolithi, urolithi composition can be (7)
carbonates,
cystine,
oxalates,
phosphates,
uric acid,
urates,
xanthine.
cholelithi s. calculi biliares
Bile stones consist of protein main substance, calcium salt, bile pigments and cholesterin. Respectively, they can be classified as calcium, pigment and mixed stones.
sialolithi s. calculi salivales
Salivary gland stones mainly consist of calcium salts and are smooth and hard.
Sometimes the nidus is a tiny shred of straw or a single grain. Cattle may have them in the pancreatic duct, horses in parotid duct.
Pseudostones consist of
feed particles that have imbued with mineral
salts.
Pseudostones are round as well, but weigh less than real stones and vary in size (2–20 cm). They build up in the colon of horses, in more rare cases in bovine rumen and intestines, and can be single or multiple in
number.
Bezoars consist of
animal hairs or vegetable fiber and are puffy. They are found in rumen of ruminants.
Bezoars of animal hairs develop when the animal preens itself or another animal.
Necrosis is
death of single cells, groups of cells, parts of an organ or even single organs in a living organism. In a necrotic tissue all vital processes have stopped.
Often necrobiosis may precede necrosis.
necrobiosis is
is the physiological death of a cell.
This is a slow lethal process, vital functions of cells and tissues extinguish slowly. Necrobiotic processes
include advanced degenerative processes in cells that terminate with cell death (necrosis). It is identified both with and without necrosis.
Apoptosis, formerly called ‘necrobiosis’ or single cell necrosis, is programmed cell death.
According to the triggering factors the following etiological forms of necrosis are specified: (5)
1) traumatic necrosis
2) toxic necrosis
3) angiogenic or circulatory
necrosis
4) trophoneurotic necrosis
5) allergic necrosis.
pyknosis
or Karyopycnosis
degenerative state of cell nucleus/ is necrosis of cell nucleus
it shrinks and wrinkles, the internal structure fades and the nucleus is coloured very intensively with nucleus staining.
karyorrhexis
destructive fragmentation of the nucleus
Chromatin is distributed irregularly in the cytoplasm.
karyolysis
dissolution of the nucleus
plasmorrhexis
Cytoplasm coagulates (plasmocoagulatio) and ruptures, and the coagulated cytoplasm fragments into granules of various sizes.
plasmolysis
contraction of cell protoplasm due to loss of water by osmosis.
detritus
dry and structureless mass
necrosis sicca s. n. coagulativa
Coagulative necrosis is coagulation of proteins of cells and ground matter, denaturalisation and dehydration of the dead tissue.
Necrotic tissues are dry, thick, clay-coloured yellow or greyish yellow.
Ischemic stroke is an example of dry necrosis and is caused by deprivation of arterial
blood flow.
Zenker’s necrosis or degeneration, waxy necrosis in muscles, is also dry necrosis.
necrosis humida s. n. colliquativa
Liquefactive necrosis occurs in tissues that contain moisture, for example brain. Degeneration softens the dead brain tissue and develops into cerebral softening, encephalomalacia.
Macroscopically the liquefactive necrosis lesions resemble cyst and are of porridge-like or semi-liquid consistency.
Gangrene is a
specific form of necrosis, transformed by external environment.
Gangrene can be dry or wet. Gas gangrene is also known.
gangraena sicca
Dry gangrene is coagulative necrosis.
The necrotic tissues have dried due to vaporized humidity. Tissues and body parts affected by dry gangrene do not decompose, they will preserve their shape, but drying
makes them smaller, harder and black in colouring (the tissues mummify).
gangraena humida
Moist gangrene develops, when bacteria from the environment infect the necrotic tissues. The process in the necrotic tissues is similar to carcass putrefaction. Dead tissues become a decomposing foul-smelling mass.
Moist gangrene develops as a complication to inflammations and necrotic processes most frequently in the uterus after a hard delivery, also in the lung tissue and intestines. Aspiration pneumonia due to foreign objects and liquids in lungs is moist gangrene.
gangraena gasea s. g. anaërobica
Gas gangrene is a separate form of gangrene, caused by anaerobic microbes. Gas gangrene is dark brown swelling in skin, connective tissue and muscles under skin. If a cut is made into the swelling, gas is emitted as bubbles.
Reactive inflammation is marked by
hyperemia in the tissue and serous liquid
and leukocytes absorbing from the blood vessels.
organisation of tissue is
The process of dead tissue being replaced with connective tissue
encapsulation could occur if
necrotic dead tissue does not absorb nor get replaced with connective tissue (organise)
a connective tissue capsula will form around the necrotic region.
If encapsulation occurs around wet necrosis (brain, for instance), what forms?
a cyst will form with the breakdown products in the cyst being gradually liquefied, absorbed and replaced by serous liquid.
With dry necrosis, calcium salts may deposit in the
necrotic lesions, and calcification (petrification, ossification) will occur.
Sometimes the dead tissue will not undergo autolysis nor replace with connective tissue, it will not encapsulate. In that case the central part of the dead tissue may separate from the living tissue after liquefication and stay
between living tissues. Such part of dead tissue, detached from healthy tissues, is called
a sequester.
It is more frequent in bone tissue and it could
eliminate itself from an organism through a fistula. But granulation tissue could also develop around such focus, and a connective tissue capsula could form, which means there will be a cavity that contains pus next to the
sequester. Sequesters could also form in soft tissues, but soft sequesters like these liquefy quickly as a rule.
Circulatory disorders are caused by changes in the amount of blood in tissues and organs. These are (6)
excessive accumulation of blood or hyperemia, insufficient supply of blood or ischemia,
haemostasis,
embolism,
infarct,
bleeding and hemorrhage.
Excessive accumulation of blood or
hyperaemia
Excessive accumulation of blood or hyperemia is too much blood in tissues and organs. Hyperemia can be arterial and venous. Venous hyperemia is more relevant in pathology.
hyperaemia arterialis s. h. activa
Arterial or active hyperemia can be general and focal. General hyperemia occurs, when the amount of circulating blood or erythrocytes has increased in the organism.
Focal arterial hyperemia is more common. It is physiological or pathological.
The more relevant types of pathological arterial hyperemia are (3)
angioneurotic, collateral and inflammatory hyperemia.
hyperaemia venosa s. h. passiva
Venous or passive hyperemia occurs, when too little blood is removed from tissues and organs, but arterial flow remains normal (or has decreased).
As a result, the amount of venous blood increases (congestion is developing). Veins and capillaries widen with venous hyperemia, blood flow slows down and the result is hypoxia, lack or reduction of oxygen flow into tissues.
The causes of venous hyperemia can be: (2)
1) central (cardiovascular deficiency), resulting in general venous hyperemia
2) peripheral (blood flow from tissues and organs is obstructed), resulting in local venous
hyperemia.
Acute congestion is the result of
short-term cardiac disorder or acute obstruction of blood outflow.
refractory ischemia
or Angiospastic ischemia
develops as a result of reflex constriction of the vasomotor centres and blood vessels under the influence of various stimuli.
Necrosis due to circulatory disorders is called an
infarction.
Stasis is
a stoppage or diminution of blood circulation.
Hypostasis is
stoppage of circulation in lower regions post mortem. Blood stops in lower tissues and organs due to its weight and
gravity.
Hypostasis can occur in a living organism due to weakness of cardial activity (hypostatic hyperemia).
Four sequential stages can be distinguished in forming a thrombus:
1) thrombocyte agglutination
2) fibrinogen coagulation
3) erythrocyte agglutination and
4) plasma protein precipitation
According to lumen thrombi are classified as:
1) mural thrombi (thrombus praemuralis), that attach to a limited patch of the inner layer of a blood vessel and
2) occluding thrombi (thrombus obturans), that completely
obstruct the lumen.
Mural thrombi form mainly in
bigger blood vessels, also heart valves, reaching the cardiac cavity.
Occluding thrombi occur in
smaller blood vessels, where they fill the whole lumen.
what distinguishes thrombi from post mortem clots
Thrombi are tightly attached to the blood vessel walls, which distinguishes them from post mortem clots that are not attached.
Thromboarteritis (thromboarteritis) is
arterial inflammation with thrombus formation.
Thrombophlebitis (thrombophlebitis) is
venous inflammation with thrombus formation.
Thromboendocarditis is
formation of a thrombus on a endocardium which also has
inflammation.
A thrombus has 3 options:
may dissolve, become organized or calcify.
thrombus Dissolution may be one of two options
aseptic (by proteolytic blood factors)
or septic
(by microbes that have penetrated thrombus mass, often producing pus).
Embolism is
partial or complete occlusion of a blood vessel lumen with a particle or substance that is not present in blood in normal
conditions.
The detached physical mass or particle involved in embolism is called
an embolus.
Embolism may be caused by (6)
parts of thrombi and necrotic tissues,
tumor cells,
fat drops that enter the blood stream from bone marrow if
there is a bone fraction,
aggregates of bacteria,
parasites and
also air bubbles that may enter blood vessels when they are injured.
Emboli obstruct arteriae and can cause
necrosis (infarctus) of the tissue or organ fed by the artery.
Emboli in organs with well-branched blood vessels may not cause mutations due to collateral circulation, that will develop.
If embolism is caused by pus, for example, with bacteria causing the inflammation, then what may develop?
abscesses may develop.
tumor cell emboli may trigger secondary tumors etc. All the
secondary tumors that develop due to pathological material spreading from the primary tumor, are called
metastases.
Infarction is
(infarctus)
a necrotic focus that has occurred in an organ, because
blood circulation in the organ has stopped.
The reasons are circulatory disturbances – thrombosis, embolism and prolonged spasm that lead to ischemia.
Infarction is an extreme result of ischemia.
the main factors for infarction are (3)
thrombosis, embolism and prolonged spasm.
By exterior qualities infarction can be classified as
infarction.
white/ischemic infarction,
red/hemorrhagic infarction
and white/ischemic infarction with hemorrhagic borders.
Infarction can also be venous.
usual infarction shape
Usually they are of triangular shape, tapered, with the pointed end towards the obstructed artery and the base towards the surface of the organ (in kidneys, spleen, lungs).
The tapered shape is due to the triangular branching of arteries.
the infarction is of irregular shape in what organs
In myocardium, intestines, the brain, the infarction is of irregular
shape, which is due to the cell structure of the blood vessels of these organs.
Two sequential stadiums can be identified in the development of
infarctions:
ischemic (pre-necrotic) and necrotic.
Ischemic phase is characterised by progressive degenerative
and necrobiotic changes, which appear and progress and are detectable by histochemical, histological and electron-microscopical study.
Necrotic phase is autolysis of dead tissue and has all the
morphological characteristics of necrosis.
Ischemic phase of infarctus is characterised by
progressive degenerative and necrobiotic changes, which appear and progress and are detectable by histochemical, histological and electron-microscopical study.
Necrotic phase of infarctus is characterized by
autolysis of dead tissue and has all the morphological characteristics of necrosis.
White infarction in animals occurs mostly in
kidneys (often dogs and horses) and spleen,
less frequently in myocardium and intestines.
Venous congestion in an organ is a contributing factor for
haemorrhagic infarctus.
Hemorrhagic infarction occurs in
lungs, intestines and spleen.
White infarction with a hemorrhagic border zone develops, when
the reflectory spasm that started with blocking the artery is replaced by paralytic widening in its branches, which results in blood filling the peripheral small vessels, leading to haemostasis and hemorrhagic diapedesis.
It is more frequent in kidneys and myocardium.
Venous infarction occurs, when the vein is
compressed fast or due to thrombosis.
Venous infarction can also be contributed by deficiencies of
anastomosis and collaterals.
In animals it occurs with uterus and bowel rotation.
Externally it resembles hemorrhagic infarction, but has an ischemic zone on the location of the rotation.
myomalacia
softening of muscle tissue
septic infarction.
due to the thrombobacterial embolus.
Septic infarctions in kidneys and spleen that occur in animals form abscesses.
If blood accumulates in tissues, it is
bruising or contusion.
Escape of blood from vessels is called extravasation (extravasatio sanguinis) and the blood outside the vessel is
extravasate.
two words for when Contusions extend under the skin or to deeper tissues
(sugillation, suffusion).
Due to contusions, localized collection of extravasated blood in an organ, space or tissue is called
a haematoma (mostly in subcutaneous connective tissue).
According to the underlying causes, there are three types of
haemorrhages and haematomas:
1) by rupture (haemorrhagia per rhexin)
2) per diabrosin (haemorrhagia per diabrosin)
3) per diapedesin (haemorrhagia per diapedesin).
(cardiac tamponade).
pericardial cavityfilled with blood
Haemorrhagia per diabrosin occurs when the wall of a blood
vessel is damaged due to
inflammations, ulcers, tumors.
Haemorrhagia per diapedesin occurs from capillaries and
arterioles due to
increased permeability, even though the walls are intact.
Diapedetic contusions may occur due to intoxications (phosphorus, arsenic), contagious diseases, venous congestion etc.
